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We reported that external dead space ventilation (EDSV) enhanced self-sustained muscle activity (SSMA) of the human soleus muscle, which is an indirect observation of plateau potentials. However, the main factor for EDSV to enhance SSMA remains unclear. The purpose of the present study was to examine the effects of EDSV-induced hypercapnia, hypoxia, and hyperventilation on SSMA. In Experiment 1 (n = 11; normal breathing [NB], EDSV, hypoxia, and voluntary hyperventilation conditions) and Experiment 2 (n = 9; NB and normoxic hypercapnia [NH] conditions), SSMA was evoked by electrical train stimulations of the right tibial nerve and measured using surface electromyography under each respiratory condition. In Experiment 1, SSMA was significantly higher than that in the NB condition only in the EDSV condition (P < 0.05). In Experiment 2, SSMA was higher in the NH condition than in the NB condition (P < 0.05). These results suggest that the EDSV-enhanced SSMA is due to hypercapnia, not hypoxia or increased ventilation.

BACKGROUND: Static stretching has been shown to reduce exercise efficiency and performance of aerobic exercises as well as decreasing the ability to generate maximum muscle force in momentary movements such as jumping. As a mechanism for the reduced efficiency, the possibility that changes in muscle fiber recruitment occur to compensate for the decrease in maximum voluntary contraction (MVC) has been suggested. We examined whether the stretching-induced decrease in exercise efficiency is accompanied by a decrease in MVC and changes in electromyo-graphic (EMG) activities of exercising muscles.METHODS: Eight healthy subjects performed 6 min of cycling exercise at 70% of maximal oxygen uptake in the conditions with and without pre-exercise static stretching (stretching condition [SC] and control condition [CC]). MVC was measured before stretching maneuvers (or the resting period in CC) and after the end of exercise. In the 6-min exercise test, respiratory parameters and EMG activities of knee extensors were measured.RESULTS: Oxygen uptake at 3 min and 6 min during the cycling exercise were higher in the SC than in the CC (P<0.05). There was no differ-ence in MVC at the end of 6 min exercise between the two conditions. Similarly, there were no differences in EMG activities during the 6-min exercise between the two conditions.CONCLUSIONS: The results suggest that pre-exercise static stretching reduces exercise efficiency independent of its negative effect on MVC exertional capacity.

We reported that external dead space ventilation (EDSV) enhanced self-sustained muscle activity (SSMA) of the human soleus muscle, which is an indirect observation of plateau potentials. However, the main factor for EDSV to enhance SSMA remains unclear. The purpose of the present study was to examine the effects of EDSV-induced hypercapnia, hypoxia, and hyperventilation on SSMA. In Experiment 1 (n = 11; normal breathing [NB], EDSV, hypoxia, and voluntary hyperventilation conditions) and Experiment 2 (n = 9; NB and normoxic hypercapnia [NH] conditions), SSMA was evoked by electrical train stimulations of the right tibial nerve and measured using surface electromyography under each respiratory condition. In Experiment 1, SSMA was significantly higher than that in the NB condition only in the EDSV condition (P < 0.05). In Experiment 2, SSMA was higher in the NH condition than in the NB condition (P < 0.05). These results suggest that the EDSV-enhanced SSMA is due to hypercapnia, not hypoxia or increased ventilation.

BACKGROUND: Increased work of breathing or fatigue of respiratory muscles has been suggested to reduce exercise performance. PURPOSE: The present study investigated the effects of continuous inspiratory resistive breathing (IRB) on the responsiveness of corticospinal pathway innervating the vastus lateralis (VL) to determine whether respiratory muscle fatigue affects the central motor output to exercising limb muscles. METHODS: Eight subjects underwent a 6-min IRB trial three times (IRB1-3) in two experiments. During each IRB trial, the subjects performed voluntary hyperventilation through a mask attached with an inspiratory resistive load (approximately 30% of maximal inspiratory pressure (Plmax)). In Experiment 1, Plmax was measured at baseline and after each IRB trial. In Experiment 2, VL responses to transcranial magnetic stimulation (motor evoked potentials (MEPs) and cortical silent periods were assessed during 5 s isometric knee extension at an intensity of 15% of the maximal voluntary contraction over the same time course as in Experiment 1. RESULTS: Plmax decreased from baseline after IRB2 and IRB3 (P < 0.05). MEPs increased from baseline after IRB1 and IRB2 (P < 0.05), whereas MEPs after IRB3 were not significantly different from baseline. Cortical silent periods did not change from baseline after IRB1 and IRB2, whereas cortical silent periods after IRB3 increased from baseline (P < 0.05). CONCLUSION: These results suggest that as inspiratory muscle fatigue progresses, the corticospinal tract controlling the lower limb muscles can shift from excitatory dominance to inhibitory dominance as a whole, affecting the central motor output to working limb muscles.

It has been shown that the tissue oxygen index (TOI) measured by near-infrared spectroscopy oscillates at very low frequencies during recovery after exercise and that this oscillation is derived from interactions among biochemical substances involved in oxidative metabolism in skeletal muscle. As a further step, we examined whether TOI in muscle interacts through oscillation with factors related to oxygen in the cardiorespiratory system. For this examination, coherence and phase difference between the TOI in the vastus lateralis and heart rate (HR) and between TOI and arterial oxygen saturation (SpO2) were sequentially determined during recovery (2–60 min) after severe cycle exercise with a workload of 7.5% of body weight for 20 s. Significant coherence between TOI and HR was obtained in the very low-frequency band (approximate range: 0.002–0.03 Hz) and in the low-frequency band (approximate range: 0.06–0.12 Hz). The phase difference was negative in the low-frequency band and positive in the very low-frequency band. The coherence between TOI and SpO2 was significant in the very low-frequency band. The phase difference was negative. There were no sequential changes in these coherences and phase differences. The results suggest that TOI in skeletal muscle interrelates with factors related to the heart and lungs.

The aim of the present study was to determine the effect of hypercapnia on motor neuromuscular activity of the human triceps surae muscle. Nine subjects participated in trials in a normal breathing condition and a CO2 rebreathing condition. In both conditions, in order to provoke self-sustained muscle activity, percutaneous electrical train stimulation was applied to the tibial nerve while each subject lay on a bed. Self-sustained muscle activity, which is an indirect observation of plateau potentials in spinal motoneurons, was measured for 30 s after the train stimulation by using surface electromyography. The sustained muscle activity was increased by CO2 rebreathing (P < 0.05). This finding suggests that motor neuromuscular activity may be linked to the respiratory system that is activated during hypercapnia.

Purpose Effort sense has been suggested to be involved in the hyperventilatory response during intense exercise (IE). However, the mechanism by which effort sense induces an increase in ventilation during IE has not been fully elucidated. The aim of this study was to determine the relationship between effort-mediated ventilatory response and corticospinal excitability of lower limb muscle during IE. Eight subjects performed 3 min of cycling exercise at 75-85 % of maximum workload twice (IE1st and IE2nd). IE2nd was performed after 60 min of resting recovery following 45 min of submaximal cycling exercise at the workload corresponding to ventilatory threshold. Vastus lateralis muscle response to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs), effort sense of legs (ESL, Borg 0-10 scale), and ventilatory response were measured during the two IEs. The slope of ventilation (l/min) against CO2 output (l/min) during IE2nd (28.0 +/- 5.6) was significantly greater than that (25.1 +/- 5.5) during IE1st. Mean ESL during IE was significantly higher in IE2nd (5.25 +/- 0.89) than in IE1st (4.67 +/- 0.62). Mean MEP (normalized to maximal M-wave) during IE was significantly lower in IE2nd (66 +/- 22 %) than in IE1st (77 +/- 24 %). The difference in mean ESL between the two IEs was significantly (p < 0.05, r = -0.82) correlated with the difference in mean MEP between the two IEs. The findings suggest that effort-mediated hyperventilatory response to IE may be associated with a decrease in corticospinal excitability of exercising muscle.

The purpose of the present study was to examine how oscillation of tissue oxygen index (TOI) in non-exercising exercise is affected during high-intensity and low-intensity exercises. Three exercises were performed with exercise intensities of 30% and 70% peak oxygen uptake ((V)over doto(2)peak) for 12 min and with exercise intensity of 70% (V)over doto(2)peak for 30 s. TOI in non-exercising muscle (biceps brachii) during the exercises for 12 min was determined by nearinfrared spectroscopy. TOI in the non-exercising muscle during the exercises was analyzed by fast Fourier transform (FFT) to obtain power spectra density (PSD). The frequency at which maximal PSD appeared (Fmax) during the exercise with 70% (V)over doto(2)peak for 12 min (0.00477 +/- 0.00172 Hz) was significantly lower than that during the exercise with 30% (V)over doto(2)peak for 12 min (0.00781 +/- 0.00338 Hz). There were significant differences in blood pH and blood lactate between the exercise with 70% V.o2peak and the exercise with 30% (V)over doto(2)peak. It is concluded that TOI in nonexercising muscle oscillates during low-intensity exercise as well as during high-intensity exercise and that the difference in Fmax between the two exercises is associated with the difference in increase in blood lactate derived from the exercise.

The aim of this study was to investigate the effects of heat exposure in the absence of hyperthermia on power output during repeated cycling sprints. Seven males performed four 10-s cycling sprints interspersed by 30 s of active recovery on a cycle ergometer in hot-dry and thermoneutral environments. Changes in rectal temperature were similar under the two ambient conditions. The mean 2-s power output over the 1st-4th sprints was significantly lower under the hot-dry condition than under the thermoneutral condition. The amplitude of the electromyogram was lower under the hot-dry condition than under the thermoneutral condition during the early phase (0-3 s) of each cycling sprint. No significant difference was observed for blood lactate concentration between the two ambient conditions. Power output at the onset of a cycling sprint during repeated cycling sprints is decreased due to heat exposure in the absence of hyperthermia.

The purpose of this study was to determine whether tissue oxygen indices (TOIs) in two muscle groups oscillated and were synchronized in repetition of impulse exercise with high intensity. Five impulse exercises of 400 watts for 10 s were repeated with intervals of 6 min. During this period, TOI was determined by near-infrared spectroscopy in the vastus lateralis and gastrocnemius muscles. TOIs in the two muscles oscillated at rest. The TOIs rapidly decreased during each impulse exercise and then recovered and overshot after each impulse. The TOIs oscillated during each interval period. During this test period, coherent and phase differences were determined. There was high coherence between TOIs in the two muscles with a peak value at 0.019 Hz. There was a phase difference of -45 +/- 32.4 degrees between TOIs in the two muscles. This phase difference corresponded to about 6 s in time scale. It seemed from this time delay that impulse exercise was not a trigger factor for the starting point of TOIs in the two muscles. It has been concluded that TOIs oscillate and are synchronized between two muscles in repetition of impulse exercise with high intensity.

The purpose of the present study was to examine how end tidal CO2 pressure (PETCO2) is controlled in impulse exercise. After pre-exercise at 25 watts for 5 min, impulse exercise for 10 sec with 200 watts followed by post exercise at 25 watts was performed. Ventilation ((V) over dotE) significantly increased until the end of impulse exercise and significantly re-increased after a sudden decrease. Heart rate (HR) significantly increased until the end of impulse exercise and then decreased to the pre-exercise level. PETCO2 remained constant during impulse exercise. PETCO2 significantly increased momentarily after impulse exercise and then significantly decreased to the pre-exercise level. PETCO2 showed oscillation. The average peak frequency of power spectral density in PETCO2 appeared at 0.0078 Hz. Cross correlations were obtained after impulse exercise. The peak cross correlations between (V) over dotE and PETCO2, HR and PETCO2, and (V) over dotE and HR were 0.834 with a time delay of -7 sec, 0.813 with a time delay of 7 sec and 0.701 with a time delay of -15 sec, respectively. We demonstrated that PETCO2 homeodynamics was interactively maintained by PETCO2 itself, CO2 transportation (product of cardiac output and mixed venous CO2 content) into the lungs by heart pumping and CO2 elimination by ventilation, and it oscillates as a result of their interactions.

Time delay in the mediation of ventilation (V. E) by arterial CO2 pressure (PaCO2) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. V. E, end tidal CO2 pressure (PETCO2) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO2 was estimated from PETCO2 and tidal volume (V-T). Results showed that predicted arterial CO2 pressure (PaCO2 pre) increased during recovery in both tests. In both tests, VE increased and peaked at the end of exercise. VE decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO2 (pre) and VE was obtained in the time delay of 7 s (r= 0.854) in test one and in time delays of 6 s (r= 0.451) and 31 s (r= 0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO2 pre drives VE with a time delay and that higher work intensity induces a shorter time delay.

The purpose of the present study was to examine 1) whether O2 uptake (VO2) oscillates during light exercise and 2) whether the oscillation is enhanced after impulse exercise. After resting for 1 min on a bicycle seat, subjects performed 5-min pre-exercise with 25 watts work load, 10-s impulse exercise with 200 watts work load and 15-min post exercise with 25 watts work load at 80 rpm. VO2 during pre-exercise significantly increased during impulse exercise and suddenly decreased and re-increased until 23 s after impulse exercise. In the cross correlation between heart rate (HR) and VO2 after impulse exercise, VO2 strongly correlated to HR with a time delay of -4 s. Peak of power spectral density (PSD) in HR appeared at 0.0039 Hz and peak of PSD in VO2 appeared at 0.019 Hz. The peak of the cross power spectrum between VO2 and HR appeared at 0.0078 Hz. The results suggested that there is an oscillation in O2 uptake during light exercise that is associated with the oscillation in O2 consumption in active muscle. The oscillation is enhanced not only by change in O2 consumption but also by O2 content transported from active muscle to the lungs.

We investigated ventilation ((V) over dotE) control factors during recovery from light impulse-like exercise (100 watts) with a duration of 20 s. Blood ions and gases were measured at rest and during recovery. (V) over dotE, end tidal CO2 pressure (PETCO2) and respiratory exchange ratio (RER) were measured continuously during rest, exercise and recovery periods. Arterial CO2 pressure (PaCO2 (pre)) was estimated from PETCO2 and tidal volume (V-T). RER at 20 s of exercise and until 50 s during recovery was significantly lower than RER at rest. Despite no change in arterialized blood pH level, PaCO2 (pre) was significantly higher in the last 10 s of exercise and until 70 s during recovery than the resting value. (V) over dotE increased during exercise and then decreased during recovery; however, it was elevated and was significantly higher than the resting value until 155 s (p<0.05). There was a significant relationship between (V) over dotE and PaCO2 (pre) during the first 70 s of recovery in each subject. The results suggest that PaCO2 drives (V) over dotE during the first 70 s of recovery after light impulse-like exercise. Elevated (V) over dotE in the interval from 70 s until 155 s during recovery might be due to neural factors.

To determine that whether arterial carbon dioxide (PaCO2) affects ventilation (VE) during recovery from impulse-like exercises of various intensities, subjects performed four impulse-like tests with different workloads. Each test consisted of a 20-sec impulse-like exercise at 80 rpm and 60-min recovery. Blood samples were collected at rest and during recovery to measure blood ions and gases. VE was measured continuously during rest, exercise and recovery periods. A significant curvilinear relationship was observed between VE and pH during recovery from the 300 and 400 watts tests in all subjects. VE was elevated during recovery from the 100 watts test despite no change in any of the humoral factors. Arterialized carbon dioxide (PaCO2) kinetics showed fluctuation, being increased at 1 min and decreased at 5 min during recovery, and this fluctuation was more enhanced with increase in exercise intensity. There was a significant relationship between VE and PaCO2 during recovery from the 300 and 400 watts tests in all subjects. The results of the present study demonstrate that pH and neural factors drive VE during recovery from impulse-like exercise and that fluctuation in PaCO2 controls VE as a feedback loop and this feedback function is more enhanced as the work intensity increases.

In order to test our hypothesis that muscle condition has an effect on the cognition of self-motion and consequently on the ventilatory response during exercise, six healthy subjects performed a moderate incremental exercise test (IET) on a cycle ergometer under two conditions [resistance exercise condition (REC) and control condition (CC)]. In the REC, resistance exercise (30 incline leg presses) was conducted during two sessions scheduled at 48 and then 24 h prior to the IET. For the CC, the subjects were instructed to refrain from participating in strenuous exercise for a period of 2 days prior to the IET. In the IET, the workload was increased from 78 to 118 W in steps of 8 W every 3 min. Although the ventilatory response during the IET was significantly higher in the REC than in the CC, there were no significant differences in cognitive indexes (RPE and awareness of change in workload) between the two conditions. In addition, the magnitude of muscle soreness was significantly higher in the REC than in the CC. However, the level of soreness in the REC was very low, and there were no significant differences in blood lactate concentration and integrated EMG between the two conditions. These results suggest that a change in peripheral neural reflex is the primary cause of increased ventilatory response to moderate exercise after resistance exercise, although the role of a cognitive element cannot be absolutely excluded.

The purpose of this study was to determine the effect of oral administration of sodium bicarbonate (NaHCO3) on surface electromyogram (SEMG) activity from the vastus lateralis (VL) during repeated cycling sprints (RCS). Subjects performed two RCS tests (ten 10-s sprints) interspersed with both 30-s and 360-s recovery periods 1 h after oral administration of either NaHCO3 (RCSAlk) or CaCO3 (RCSPla) in a random counterbalanced order. Recovery periods of 360 s were set before the 5th and 9th sprints. The rate of decrease in plasma HCO3− concentration during RCS was significantly greater in RCSAlk than in RCSPla, but the rates of decline in blood pH during the two RCS tests were similar. There was no difference between change in plasma lactate concentration in RCSAlk and that in RCSPla. Performance during RCSAlk was similar to that during RCSPla. There were no differences in oxygen uptake immediately before each cycling sprint (preVO2) and in SEMG activity between RCSAlk and RCSPla. In conclusion, oral administration of NaHCO3 did not affect SEMG activity from the VL. This suggests that the muscle recruitment strategy during RCS is not determined by only intramuscular pH.